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PR3151 (cleefy) > IC14 PR3151 SSTI > Flashcards

IC14 PR3151 SSTI Flashcards

1
Q

(Relate the anatomical site to the type of SSTI)
Epidermis

A

Impetigo

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2
Q

(Relate the anatomical site to the type of SSTI)
Dermis

A

Ecthyma, erysipelas

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3
Q

(Relate the anatomical site to the type of SSTI)
Hair follicles

A

Furuncles
Carbuncles (cluster of furuncles)

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4
Q

(Relate the anatomical site to the type of SSTI)
SubQ fat

A

Cellulitis

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5
Q

(Relate the anatomical site to the type of SSTI)
Fascia (surrounds blood vessels)

A

Necrotizing fasciitis

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6
Q

(Relate the anatomical site to the type of SSTI)
Muscle

A

Myositis

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7
Q

(Relate the anatomical site to the type of SSTI)
Skeletal muscle

A

Pyomyositis (purulent infection of skeletal muscle, often with abscess formation

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8
Q

Factors that impair skin barrier function (x9)

A

age (very young and old)
infection
phy dmg (pressure, friction, lacerations)
phy environment (contact w urine faeces sweat and chronic wound fluid)
ischaemia (lack of perfusion)
diseases (diabetes, etc)
drugs (immunosupps, SGLT2i, etc)
pH (unbalanced detergents, phy envi)
excess soap and detergent use

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9
Q

What are the protective mechanisms of the skin against SSTIs?

A

1) normal skin function acts as a protective barrier against infections.

2) continuous renewal of epidermal layer results in shedding of keratocytes and skin microbiota

3) sebaceous secretions inhibit growth of many bact and fungi

4) normal commensal skin microbiome prevents colonisation and overgrowth of more pathogenic strains.

5) others: pH (acidic environment of the skin), AMP anti-microbial peptides

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10
Q

What are the three risk factors for SSTIs?

A

1) disruption of the skin barrier

2) conditions that predispose to infection

3) history of cellulitis

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11
Q

how does a disruption of skin barrier become a risk factor for SSTI?

describe some of the conditions for the above^

A
  • traumatic
  • non-traumatic: ulcer, tinea pedis, dermatitis, toe web intertrigo, chemical irritants.
  • impaired venous and lymphatic drainage (poor flow preventing rescue agents from flowing there and fight invaders + retention and overgrowth of organism causing it to invade): saphenous venectomy, obesity, chronic venous insufficiency.
  • peripheral artery disease
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12
Q

what are the conditions (and drugs)that predispose to infection of sstis (risk factor)

A
  • diabetes, cirrhosis, neutropenia, hiv, transplantation and immunosuppressive meds
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13
Q

methods to prevent SSTIs?

A

1) good care to maintain skin integrity: good wound care, tx of tinea pedis, preventing dry cracked skin, good foot care for DM patients to prevent wounds and ulcers.

2) identify any predisposing factors and treat at same time of initial diagnosis to reduce risk for recurrence.

3) acute traumatic wounds irrigated, foreign objects removed, devitalised tissues debrided (source control).

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14
Q

what history taking should be done before diagnosis of SSTI?

A

underlying diseases

recent trauma, bites, burns, water exposure

animal exposure

travel history

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15
Q

HOW should culture sample be collected for SSTIs?

A

1) deep in the wound after cleansing surface
2) base of a closed abscess, where bact grow, rather than surface
3) curettage (debride top) instead of wound swab or irrigation

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16
Q

when to collect blood culture for ssti?

A

when there are marked systemic symptoms of infection or the patient is immunocompromised

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17
Q

when and what culture samples should not be collected for sstis?

A

mild and superfiical infections where the skin commensal bact may be taken instead

wound swabs because it may be difficult to obtain representative sample.

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18
Q

what is the clinical presentation of impetigo?

A

begins as erythematous papules that rapidly evolve into vesicles and pustules that rupture, with the dried discharge forming honey-colored crusts on an erythematous base.

Usually on exposed areas of body (face and extremities).

Lesions well localised, frequently
many, bullous or non bullous in appearance.

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19
Q

what is the clinical presentation of ecthyma?

A

ulcerative form of impetigo in which the lesions extend through the epidermis and deep into the dermis.

Pruritis is common, scratching may further spread
infection

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20
Q

what is the clinical presentation of furuncle?

A

an infection of the hair follicle in
which purulent material extends through the dermis into
the subcutaneous tissue, where a small abscess forms

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21
Q

what is the clinical presentation of carbuncle?

A

formed when furuncles coalesce and extent
into subcutaneous tissues.

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22
Q

what is the clinical presentation of skin abscess?

A

collections of pus within the dermis and
deeper skin tissues. Skin abscesses manifest as painful, tender, fluctuant and erythematous nodules

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23
Q

what is the clinical presentation of erysipelas?

A

affects upper dermis; Fiery red, tender,painful plaque (raised above surrounding skin) with well‐demarcated edges.

Common on face, also lower extremities.

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24
Q

what is the clinical presentation of cellulitis ?

A

Involves deeper and subcutaneous fats.

Usually presents as an acute, diffuse, spreading, nonelevated, poorly demarcated area of erythema.

Relatively rapid onset/progression.

Almost always unilateral.

Fever in 20–70% of patients.

It is typically found on the lower extremities, although it can appear on any area of the skin.

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25
Q

what are the complications of cellulitis and erysipelas

A

BET LONG

Bacteremia, Endocarditis, Toxic shock, Lymphedema, Osteomyelitis,
Necrotizing soft‐tissue infections, Glomerulonephritis

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26
Q

what are some cellulitis mimickers and how to manage?

A

deep venous thrombosis, calciphylaxis, stasis dermatitis, hematoma, erythema migrans, cellulitis

just give a short course of narrow spectrum gram + and see whether patient improves. if no, explore further causes.

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27
Q

what are the likely pathogens for impetigo (non bullous)?

A

staphylococci and streptococci

usually beta hemolytic strep (A-C, G)

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28
Q

what are the likely pathogens for impetigo (bullous)?

A

toxin-producing strains of s.aureus

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29
Q

what are the likely pathogens for ecthyma?

A

usually grp A strep (strep pyrogenes)

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30
Q

what are the likely pathogens for non-purulent SSTI (cellulitis and erysipelas)?

A

mainly beta haemolytic strep (grp A-C,G), but usually grp A (strep pyrogenes)

S.aureus possible but less frequent.

Others (not common): aeromonas, vibrio vulnificus, and pseudomonas with (water exposure).

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31
Q

what are the likely pathogens for purulent SSTI (furuncles, carbuncles, skin abscess, purulent cellulitis)?

A

mainly s.aureus

sometimes beta haem strep (A-C,G)

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32
Q

what are some pathogenic characteristics of skin abscesses involving the peri oral, perirectal, vulvovaginal areas?

A

common to see isolation of multiple organisms including gram (-) and anaerobes.

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33
Q

CA-MRSA epidemiology?

A

Not common in SG, common in the US.

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34
Q

CA-MRSA virulence profile?

A

Presence of
- panton valentine leucocidin (PVL)
- SCCmecIV or staphylococcal chromosomal casette.

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35
Q

What are some risk factors for CA-MRSA?

A

contact sports, military personnel, IV drug abusers, prison inmates

overcrowded facilities, close contact and lack of sanitation.

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36
Q

What is the susceptibility of CA-MRSA?

what drug works against CAMRSA

A

oral non-beta lactams

  • clindamycin
  • cotrimox
  • doxycycline
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37
Q

what is the definition of HA-MRSA?

A

this is an mrsa infection that occurs

> 48h following hospitalisation
OR
outside of the hospital within 12 months of exposure to healthcare

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38
Q

how does HA-MRSA spread in the healthcare setting?

A

MRSA able to form biofilm on devices

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39
Q

What are the risk factors of HA-MRSA

A

abx use, recent hosp or surgery, prolonged hosp, intensive care, hemodialysis,
proximity to others with MRSA colonisation or infectoin

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40
Q

what abx to use for the treatment of impetigo (mild, limited lesions)?

A

topical mupirocin BD x 5days

41
Q

what is the efficacy of mupirocin to pathogens (gram positive cocci vs enterococci vs gram neg vs MRSA)

A

highly effective against gram postive cocci esp s.aureus
useful for erradication of nasal staphyloccal carriage

not effective vs enterococci and gram negs

MRSA resistance a concern

42
Q

(culture directed) (MSSA))

what abx to use for the treatment of impetigo and ecthyma (multiple lesions)?

A

PO cephexin or cloxacillin x 7days

43
Q

(empiric tx)

what abx to use for the treatment of impetigo and ecthyma (multiple lesions)?

include length of treatment

A

NO penicillin allergy:
- PO Ceph or cloxacillin x 7days

penicillin allergy:
- PO clindamycin x 7days

44
Q

(culture directed) (s pyrogenes)

what abx to use for the treatment of impetigo and ecthyma (multiple lesions)?

include length of treatment

A

PO penicillin V or amoxicillin x 7days

45
Q

what is the mainstay of treatment for purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?

A

incision and drainage (I&D)

46
Q

when do you use adjunctive systemic abx for purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?

A

when
- unable to drain completely
- lack of response to I & D
- extensive disease involving several sites
- extremes of age
- immune suppressed
- signs of systemic illness (SIRS ≥2 pts)

47
Q

What is the SIRS criteria for purulent SSTI

A

Temperature >38 or <36
HR >90
RR > 34
WBC > 12x10^9 or <4x10^9

48
Q

what is the (empiric) general treatment for mild infection of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?

A

I and D or warm compress

49
Q

what is the (empiric) general treatment for moderate infection (w systemic symptoms) of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?

A

I&D plus oral abx
- PO cloxacillin, cephalexin
OR
- PO clindamycin (penicillin allergy)

50
Q

what is the severity classification for purulent SSTIs?

A

mild = no systemic infection

moderate - severe = systemic symptoms (classification with the SIRS scale, ≥2 points qualifies) and other risk factors (recall)

51
Q

what is the (empiric) general treatment for severe infection of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?

A

I&D plus IV abx
- IV cloxacillin or cefazolin or clindamycin or vancomycin

52
Q

what is the (empiric) (MRSA) treatment of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?

IF GOT MRSA RISK FACTORS

include length of treatment

A

mild
PO cotrimox, doxy, clindamycin x5-10 days

mod-severe
IV Vanco, dapto, linezolid

reserve dapto and linezolid is VRE or allergy

53
Q

what is the (empiric) (including gram neg anaerobic) treatment of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?

Recall AND state when you treat for gram neg and anaerobe

(simple)

A

PO amoxiclav x5-10 days

  • recall that this is better for skin abscess near the perioral, perirectal, vulvovaginal…
54
Q

(long hospital stay and high resistance risk)

Recall AND state when you treat for gram neg and anaerobe

SEVERE PURULENT SSTI

A

piptazo

55
Q

what is the (empiric) (including gram neg anaerobic) treatment of purulent SSTIs (furuncles, carbuncles, skin abscess, purulent cellulitis)?

Recall AND state when you treat for gram neg and anaerobe

(very sick, i.e., severe illness)

A

carbapenem

to cover for ESBL, amp c producing

56
Q

what is the (empiric) treatment of mild, non-purulent SSTIs (cellulitis, erysipelas)?

i.e., no systemic signs of infection

A

ORAL abx
penicillin V, cephalexin, cloxacillin
x5-10days

penicillin allergy
clindamycin
x5-10days

57
Q

what is the (empiric) treatment of moderate, non-purulent SSTIs (cellulitis, erysipelas)?

i.e., systemic signs with some purulence

consider additional….

A

IV abx
cefazolin, cloxacillin x5-10days

penicillin allergy
clindamycin x5-10days

add cipro if water exposure

58
Q

when there is moderate non purulent SSTI with water exposure,

what are the extra organisms to cover for and what abx to add on for empiric tx?

A

vibrio, aeromonas, pseudomonas x5-10days

include ciprofloxacin

59
Q

what is the (empiric) treatment of severe, non-purulent SSTIs (cellulitis, erysipelas)?

include additional therapy for MRSA risk factor coverage

add reason for change in reigmen

A

IV antibiotics: piptazo, cefepime, merepenem x5-10days (increase to 14 immunocompromised)

add vancomycin, daptomycin, linezolid if MRSA risk factor.

to broaden coverage and include risk for necrotizing infections

60
Q

what are the signs/factors for severe non purulent sstis?

A

systemic signs of infection, failed oral therapy, immunocompromised.

61
Q

what are the non-phx measrues for nonpurulent SSTI?

A

rest and limb elevation (drainage of edema and inflammatory substances)

Treat underlying conditions eg tinea pedis, skin dryness, limb edema

62
Q

what are the goal and monitoring parameters for ssti?

A

1) resolution of s/sx
- improvement 48-72h
- no progression of lesion or development of complication
- switch to oral once better
- if no response 2-3 days, reassess condition + choice of abx

2) no need for repeat bact culture.

3) no ADR.

63
Q

define DFIs in words

A

soft tissue or bone infections below the malleolus usually involving bacterial colonization of ulcers and wounds

64
Q

what are the complications of DFIs?

A

hospitalisation

osteomyelitis

eventual amputation

65
Q

what is the pathophysiology of DFIs?

A

1) Neuropathy
Peripheral: ↓ pain
sensation and altered
pain response
* Motor:muscle imbalance
* Autonomic: ↑ dryness,
cracks and fissures

2) Vasculopathy
* Early atherosclerosis
* Peripheral vascular
* disease
* Worsened by
hyperglycemia and
hyperlipidemia

3) Immunopathy
* Impaired immune
response
* ↑ susceptibility to
infections
* Worsened by
* hyperglycemia

66
Q

what is the criteria for DFI?

A

purulent discharge

OR

≥2 s/sx of inflammation:
erythema, warm, tenderness, pain, induration

67
Q

what is the clinical presentation and progression of DFIs?

A

Superficial ulcer,
mild erythema –> Deep tissue infection, extensive erythema –> Infection of bone and fascia, purulent discharge –> Localized gangrene

68
Q

what is the evolution of DFIs?

A

erythema (day 1), blisters (day 3), a necrotizing abscess (day 6), and
wound infection requiring surgery (day 10).

69
Q

what are the causative organisms for DFIs?

include gram positive, gram negative, and anaerobes

A

usually polymicrobial

gram positive most common: S.aureus and strep spp

gram negative: EKP
Pseudomonas less common

anaerobes: peptostreptococcous, veillonella, bacteriodes

70
Q

when would there be presence of gram negs in DFIs?

A

chronic wounds/wounds treated with abx

71
Q

when would there be presence of anaerobes in DFIs?

A

ischaemic or necrotic wounds

72
Q

cultures for DFIs? when and how? consider the different classifications

A

Mild DFIs
* Optional

Moderate – severe DFIs
* Deep tissue cultures after cleansing and before starting antibiotics (if possible)
* Avoid skin swabs

Do not culture uninfected wounds

73
Q

what are pseudomonal risk factors for DFIs

A

frequent water exposure, warm climate

74
Q

when to cover for psuedomonas in DFIs?

A

risk factors

severe infection

or
mod infection with risk factors?

75
Q

what is the classification for MODERATE DFI?

A

Infection of deeper tissue (e.g. bone, joints); or
If erythema: > 2 cm around ulcer

No signs of systemic infection

76
Q

what is the classification for MILD DFI?

A

Infection of skin and SC tissue
+
If erythema: ≤ 2 cm around ulcer
+
No signs of systemic infection

77
Q

what is the classification for SEVERE DFI?

A

Infection of deeper tissue (e.g. bone, joints); or
If erythema: > 2 cm around ulcer

+
Sign(s) of systemic infection

78
Q

what are the organisms to cover for MILD DFI?

A

Streptococcus spp +
S. aureus

79
Q

what are the organisms to cover for MODERATE DFI?

A

Streptococcus spp +
S. aureus +
gram‐negatives
(±P. aeruginosa) +
anaerobes

80
Q

what are the organisms to cover for SEVERE DFI?

A

Streptococcus spp +
S. aureus +
gram‐negatives
(include P.aeruginosa) +
anaerobes

81
Q

what is the empiric tx for MILD DFI?

A

PO Antibiotics
* Cephalexin
* Cloxacillin
* Clindamycin

If MRSA risk factor(s), use PO:
* Co‐trimoxazole
* Clindamycin
* Doxycycline

82
Q

what is the empiric tx for MODERATE DFI?

A

Initial IV Antibiotics
* Amoxicillin/clavulanate
* Cefazolin (more ideal because 1st and 2nd gen)/Ceftriaxone + Metronidazole

IfMRSA risk factor(s), addIV:
* Vancomycin
* Daptomycin
* Linezolid

83
Q

what is the empiric tx for SEVERE DFI? (need to expand the spectrum)

A

Initial IV Antibiotics
* Piperacillin‐tazobactam
* Cefepime + metronidazole
* Meropenem
* Ciprofloxacin + clindamycin

IfMRSA risk factor(s), addIV:
* Vancomycin
* Daptomycin
* Linezolid

84
Q

what are some adjunctive measures to DFI

A

1) wound care
- debridement
- offloading
- dressing that promotes wound healing and exudate removal

2) optimal glycaemic control

3) foot care
- daily inspections
- prevent wounds and ulcers

85
Q

how to diagnose and confirm infection for SSTI

A

based on history and physical examination

generally mild and superficial infections do not require any culture

take wound culture only if it fulfills any of the three criteria

take blood culture only if systemic symptoms or patient is immunocompromised

86
Q

how to differentiate the severity non-purulent SSTIs? ie mild moderate severe

A

mild: no systemic symptoms

moderate: systemic symptoms and some purulence

severe: systemic symptoms with PO treatment failure, immunocompromised/suppressed

87
Q

what are the addional pathogens to cover for the different severities of non-purulent SSTIs?

A

moderate: include MSSA coverage.
severe: broader coverage and explore possibility of necrotising infections

88
Q
A
89
Q

what are the 4 synergistic factors to pressure ulcers

A

friction
shearing
pressure
moisture

90
Q

what are the risk factors for pressure ulcers

A

Reduced mobility – E.g. spinal cord injuries, paraplegic

Debilitated by severe chronic diseases – E.g. multiple sclerosis, stroke, cancer

Reduced consciousness

Sensory and autonomic impairment
– Incontinence

Extremes of age

Malnutrition

91
Q

what is the criteria for pressure ulcer infection

A

1) purulent discharge
OR
2) ≥2 of the following:
- erythema
- tenderness
- pain
- induration
- warmth

92
Q

what is the clincal presentation of pressure ulcer (4 stages)

A

stage 1:
- epidermis abrasion
- irregular area of tissue swelling
- no open wound

stage 2:
- dermis
- open wound

stage 3:
- subQ
- open sore or ulcer

stage 4:
- deeper tissue (joints, muscle, bone)
- deep sore or ulcer

93
Q

what are the pathogens for pressure ulcer

A

similar to DFI
polymicrobial

94
Q

how to culture for pressure ulcers

A

deep tissue culture or biopsy specimens
avoid skin swabs

95
Q

adjunctive measures for pressure ulcers?

A

1) debridement of necrotic/infected tissue
2) local wound care
- normal saline preferred
- avoid harsh chemicals
3) relief of pressure
- turn/reposition every 2h

96
Q

what is the dosing for daptomycin

A

4-6mg/kg q24

97
Q

what is the dosing for linezolid

A

600mg q12

98
Q

how to classify the severity of non-purulent SSTIs?

A

mild: no systemic symptoms
moderate: systemic symptoms with some purulence of the wound
severe: systemic symptoms with failed oral treatment or immunocompromised/suppressed.

99
Q

what is the reason for changing the drug regimen for severe (nonpurulent) SSTI?

A

broaden the spectrum of activity
+
potentially cover for necrotising infections (typically anaerobic bacteria)

PR3151 (cleefy) (12 decks)

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